The gamma-radiation response of stationary and budding cells of wild-type diploid strains (RAD) and radiation-sensitive strains rad2, 6, 9, 18, 50-55, 57 and rec4 was studied. As compared with the wild-type strains, mutants generally showed enhanced sensitivity in both stages of the cell cycle. Budding-cell resistance was totally absent from rad50-55 strains. Mutants rad6, 9 and 18 showed some degree of budding-cell resistance. The response of rad2 and rec4 strains was identical with that of the corresponding wild-type strains. These results suggest that the pathway dependent upon the expression of RAD50-55 loci functions more efficiently in budding cells compared with the pathway dependent on RAD2 and RAD6, 9 and 18 loci. Recombination between sister chromatids appears to play an important role in budding-cell resistance, and this process is under the control of the RAD52 repair pathway. The relationship between the repair pathways associated with budding-cell resistance and post-irradiation cellular recovery (LHR) is discussed.
|Evidence ID||Analyze ID||Interactor||Interactor Systematic Name||Interactor||Interactor Systematic Name||Type||Assay||Annotation||Action||Modification||Phenotype||Source||Reference||Note|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Gene Ontology Term||Gene Ontology Term ID||Qualifier||Aspect||Method||Evidence||Source||Assigned On||Annotation Extension||Reference|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Phenotype||Experiment Type||Experiment Type Category||Mutant Information||Strain Background||Chemical||Details||Reference|
|Evidence ID||Analyze ID||Regulator||Regulator Systematic Name||Target||Target Systematic Name||Experiment||Assay||Construct||Conditions||Strain Background||Reference|